Chlamydia trachomatis is an obligate intracellular bacterial pathogen and a leading cause of sexually transmitted bacterial diseases. C. trachomatis organisms have adapted an intravacuolar replication life cycle and can persist in the infected hosts for a long period of time. The chlamydial persistence, a major cause of chlamydia-induced diseases in humans, may be due to chlamydial ability to evade host immune responses. T cell-mediated immunity plays important roles in controlling intracellular infections. Chlamydia has evolved various strategies for evading host defense, including inhibition of phagolysosomal fusion, alteration of host cell signaling pathways and inhibition of MHC antigen presentation. Research work from Dr. Zhong's lab is focused on understanding how chlamydia evades host immune mechanisms. After correlating the chlamydial suppression of MHC antigen expression with chlamydial degradation of host transcription factors, Dr. Zhong's lab has identified a chlamydia-secreted protein designated as CPAF (chlamydia-specific protease/proteasome-like activity factor) that is responsible for the chlamydial degradation of host transcription factors required for MHC gene activation. Interestingly, CPAF is synthesized as a 70kDa proprotein and rapidly processed into a 29 kDa N-terminal (CPAFn) and a 35kDa C-terminal (CPAFc) fragments. The CPAFn and c fragments form functional and stable intramolecular dimers. Dr. Zhong's lab will continue to understand the mechanisms of CPAF activation and activity using various biochemical, immunological, molecular and cellular approaches. These studies will provide important knowledge for developing strategies to prevent/block chlamydial immune evasion.